Akuu­tin ai­vo­val­ti­mo­tu­kok­sen las­ki­mon­si­säis­tä liuo­tus­hoi­toa voi­daan an­taa nel­jän ja puo­len tun­nin ku­lues­sa oi­rei­den alus­ta. Hoi­to on aloi­tet­ta­va he­ti, kun vas­ta-ai­heet on pois­sul­jet­tu. Jos po­ti­laan ai­vo­ve­ren­kier­to­häi­riön oi­reet ovat vai­keat, ei suu­ren ai­vo­val­ti­mon tu­kok­sen las­ki­mon­si­säi­nen liuo­tus­hoi­to yleen­sä rii­tä. Sen li­säk­si har­ki­taan en­do­vas­ku­laa­ri­hoi­to­na lä­hin­nä me­kaa­nis­ta trom­bek­to­miaa kuu­den tun­nin ku­lues­sa. En­do­vas­ku­laa­ri­hoi­toa har­ki­taan myös sil­loin, kun las­ki­mon­si­säi­sel­le liuo­tus­hoi­dol­le on vas­ta-ai­he: INR-ar­vo yli 1,7 tai po­ti­las käyt­tää sään­nöl­li­ses­ti uut­ta ve­re­no­hen­nus­lää­ket­tä da­bi­gat­raa­nia, ri­va­rok­sa­baa­nia tai ­apik­sa­baa­nia. Pää­tös en­do­vas­ku­laa­ri­hoi­don aloit­ta­mi­ses­ta teh­dään ylio­pis­to­sai­raa­las­sa mo­niam­ma­til­li­ses­ti, ja toi­men­pi­teen ai­hees­ta päät­tää neu­ro­lo­gi yh­des­sä sen suo­rit­ta­van ra­dio­lo­gin kans­sa. Hoi­dos­ta on an­net­tu uu­si oh­jeis­tus, jo­ka kos­kee neu­ro­lo­gian päi­vys­tä­jien li­säk­si myös päi­vys­tyk­sen eri­koi­sa­laa, ku­ten kes­kus­sai­raa­la­ta­soi­sia päi­vys­tä­jiä. Päi­vys­tyk­sel­li­seen AVH-hoi­toon lä­het­tä­mi­sen kri­tee­rit säi­ly­vät en­nal­laan ja hoi­don va­lin­taan ote­taan kan­taa ylio­pis­to­sai­raa­loi­den päi­vys­tys­pis­teis­sä.

Hemostasis is a highly regulated process, which enables the repair of damaged blood vessels by clotting but also keeps the blood fluid and removes blood clots when they are no longer needed. There is a variety of medical conditions that could lead to hemostatic malfunction, manifesting in thrombosis and/or bleeding. The aim of this study was to get acquainted with these conditions and the fundamental laboratory methods for screening hemostasis. Another goal was to study APAC variants in these selected test methods. APACs are semisynthetic molecule complexes consisting of human serum albumin (HSA) core and tailored number of covalently bound UFH chains. In several animal models, APACs have established both antiplatelet (AP) and anticoagulant (AC) functions. They target and act locally at the vascular injury site. We used 7 APAC variants differing at their coupling level of UFH (CL). We chose test methods to assess the intrinsic and common coagulation pathways, the activity and concentration of thrombin in clotting plasma, interactions between different agents in coagulation and the ability of collagen to induce platelet activation and aggregation. The chosen methods were Activated Partial Thromboplastin Time (APTT), thrombin time, Rotational Tromboelastometry (ROTEM), the Calibrated Automated Thrombogram (CAT) and Collagen-induced Platelet Aggregation in Platelet-rich plasma (Aggregometer, AggRAM). Generally, all studied APAC variants show dose-dependent inhibition of coagulation that is at least similar, but mostly more efficient compared with plain UFH. At the concentration corresponding to clinically relevant heparin concentration (3 µg/ml), APACs prolong the coagulation globally. At low concentrations they are more potent anticoagulants and thrombin inhibitors than UFH and also inhibit platelet procoagulant activity (PCA). Further studies are needed, however, the results support data that APACs are promising targets for the future drug development.

COVID-19-infektioiden estämiseen kehitetyt adenovirusvektorirokotteet aiheuttavat erittäin harvinaisena haittavaikutuksena vaikeita hyytymishäiriöitä, joissa kehittyy verihiutaleita aktivoivia vasta-aineita. Tilan kansainvälinen nimitys on vaccine-induced immune thrombotic thrombocytopenia (VITT) tai tromboottinen trombosytopeeninen oireyhtymä (TTS), jolle ominaisia ovat trombosytopenia, positiiviset verihiutaletekijä 4 (PF4) -hepariinivasta-aineet ilman hepariinin käyttöä sekä valtimo- ja laskimotukokset. Hyytymishäiriön nopea diagnosointi on tärkeää, sillä tilaan liittyy jopa 40 %:n kuolleisuus. Hoidon kulmakivet ovat antikoagulaatio muilla kuin hepariinivalmisteilla ja suonensisäisen immunoglobuliinin antaminen trombosyyttiaktivaatiota aiheuttavien vasta-aineiden syrjäyttämiseksi.

Although endovascular therapy has been proven safe and has become in many centers the primary method of treatment for intracranial aneurysms, the long-term durability of endovascular embolization remains a concern; at least for some aneurysms despite initial good result. While healing after clipping relies on mechanical occlusion, restoration after endovascular occlusion mainly requires the induction of a biological response. Healing after embolization depends on the growth of new tissue over the thrombus formed by the embolization material, or alternatively, on the organization of thrombus into fibrous tissue. This review highlights the fundamental importance of aneurysm wall biology on the healing process and long-term occlusion after intracranial aneurysm (IA) treatment. It seems likely that the effect of luminal thrombus on the IA wall, as well as the IA wall condition at the time of thrombosis, determine if thrombus organizes into scar tissue (neointima formation by infiltration of cells originating from the IA wall) or if the wall undergoes continuous remodeling, which is primarily destructive (loss of mural cells). In the latter, intraluminal thrombus organization fails and the impaired healing increases the chance of recurrence. Mechanisms underlying IA reopening, the influence of intraluminal thrombosis on the IA wall, and clinical implications of the IA wall condition are discussed in detail, along with how knowledge of IA wall biology can offer new solutions for IA treatment and affect the patient selection for and follow-up after endovascular treatment.

Background Venous thromboembolism (VTE) and bleeding are serious and potentially fatal complications of surgical procedures. Pharmacological thromboprophylaxis decreases the risk of VTE but increases the risk of major post-operative bleeding. The decision to use pharmacologic prophylaxis therefore represents a trade-off that critically depends on the incidence of VTE and bleeding in the absence of prophylaxis. These baseline risks vary widely between procedures, but their magnitude is uncertain. Systematic reviews addressing baseline risks are scarce, needed, and require innovations in methodology. Indeed, systematic summaries of these baseline risk estimates exist neither in general nor gynecologic surgery. We will fill this knowledge gap by performing a series of systematic reviews and meta-analyses of the procedure-specific and patient risk factor stratified risk estimates in general and gynecologic surgeries. Methods We will perform comprehensive literature searches for observational studies in general and gynecologic surgery reporting symptomatic VTE or bleeding estimates. Pairs of methodologically trained reviewers will independently assess the studies for eligibility, evaluate the risk of bias by using an instrument developed for this review, and extract data. We will perform meta-analyses and modeling studies to adjust the reported risk estimates for the use of thromboprophylaxis and length of follow up. We will derive the estimates of risk from the median estimates of studies rated at the lowest risk of bias. The primary outcomes are the risk estimates of symptomatic VTE and major bleeding at 4 weeks post-operatively for each procedure stratified by patient risk factors. We will apply the Grading of Recommendations Assessment, Development and Evaluation (GRADE) approach to rate evidence certainty. Discussion This series of systematic reviews, modeling studies, and meta-analyses will inform clinicians and patients regarding the trade-off between VTE prevention and bleeding in general and gynecologic surgeries. Our work advances the standards in systematic reviews of surgical complications, including assessment of risk of bias, criteria for arriving at the best estimates of risk (including modeling of the timing of events and dealing with suboptimal data reporting), dealing with subgroups at higher and lower risk of bias, and use of the GRADE approach. Systematic review registration PROSPERO CRD42021234119

Tylpät kaulasuonivammat ovat harvinaisia, mutta todennäköisesti alidiagnosoituja. Ne ovat yleensä suuren vammaenergian aiheuttamia. Oireet johtuvat iskeemisistä aivotapahtumista ja voivat vakavuudeltaan vaihdella huomattavasti sekavuudesta halvausoireisiin. Kaulasuonivamma ja verenvuoto voivat myös aiheuttaa painetta ympäröiviin kudoksiin ja ahtauttaa hengitysteitä. Diagnoosi tehdään kaulavaltimoiden TT-angiografialla. Hoidossa pyritään ehkäisemään verisuonen hyytyminen umpeen ja embolioiden muodostuminen. Endovaskulaarisiin tai avotoimenpiteisiin päädytään hyvin harvoin.